Programa de Pós-Graduação em Oncologia e Ciências Médicas - PPGOCM/NPO
URI Permanente desta comunidadehttps://repositorio.ufpa.br/handle/2011/4631
O Programa de Pós-Graduação em Oncologia e Ciências Médicas (PPGOCM) integra o Núcleo de Pesquisas em Oncologia (NPO) da Universidade Federal do Pará (UFPA). Trata-se do único centro de referência em pesquisa e formação de recursos humanos stricto sensu na área de oncologia na região Norte do Brasil. Os outros centros se concentram nas cidades do Rio de Janeiro e São Paulo.
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Item Acesso aberto (Open Access) Análise de citocinas no soro de pacientes com câncer gástrico(Universidade Federal do Pará, 2017-08-16) HAGE, Pedro Antônio Mufarrej; CALCAGNO, Danielle Queiroz; http://lattes.cnpq.br/1326603355062154Despite the reduction in the worldwide incidence of gastric cancer, this neoplasm remains the second largest cause of cancer death in the world. Late diagnosis occurs mainly due to the absence of symptoms or the presence of non-specific symptoms in the early stages of the disease. In this case, few effective therapeutic options are available, resulting in high rates of morbidity and mortality. The continuous study of new strategies for the early diagnosis, definition of the prognosis and identification of new therapeutic methods is of great interest in this neoplastic type. In the present study was quantified inflammatory proteins candidate to biomarkers in the serum of 19 patients with gastric adenocarcinoma before surgical resection and 13 healthy individuals as control. The methodology used for quantification of proteins was the MAGPIX system and panels of cancer biomarkers inventoried by the manufacturer (Bio-Plex Pro Human Pro-Cytokine, Chemokine and Growth Factors). In the comparison between patients with gastric adenocarcinoma and control group was observed the levels of IL-1β, IL-1RA, IL-2, IL-6, IL-8, IL-10, IL-12, IL-15, G-CSF, GM-CSF, IFN-γ, MIP1α, RANTES and VEGF were higher in serum of gastric adenocarcinoma patients. According clinicopathological characteristics, was observed elevated levels of IL-5, IL-7, IL-10 and IL-17A in diffuse-type gastric adenocarcinoma in relation intestinal-type. In addition, the association of the expression of the cytokines studied with overall survival (OS) and relapse-free survival (PFS) were performed using the KM Plotter Online Tool. Overexpression of G-CSF, GM-CSF and VEGF in tumor was associated with lower OS and PFS of gastric cancer patients. However, the overexpression of IL-10 was associated only with PFS. Thus, we can conclude that the IL-1β, IL-1RA, IL-2, IL-6, IL-8, IL-10, IL-12, IL-15, G-CSF, GM-CSF, IFN-γ, MIP1α, RANTES and VEGF cytokines are potential biomarkers of gastric cancer, and diffuse-type adenocarcinoma can related to a greater inflammatory response than intestinal-type. Survival analysis suggests that elevated levels of IL-10, G-CSF, GM-CSF and VEGF in serum are potential biomarkers of prognosis in gastric cancerpatients.Item Acesso aberto (Open Access) Avaliação da atividade antineoplásica dos fármacos metformina e mebendazol isolados e em associação em linhagem celular de câncer(Universidade Federal do Pará, 2018) SILVA, Karla de Assis; KHAYAT, André Salim; http://lattes.cnpq.br/6305099258051586Gastric cancer will account for 782,685 deaths worldwide in 2018, being the fifth most common cause of cancer in the world and a fourth in Brazil. For example, the diagnosis of pathognomonic cases, the diagnosis of gastric cancer occurs late in most cases. In addition, this is a series of patients with chemotherapy and radiotherapy, being a resection surgery that offers the greatest healing potential. Adenocarcinoma is the most common subtype of lung cancer, with incidence greater than 90%. The risk factors for the pathology are multiple and cover the genetic, environmental and food. The drugs metformin and mebendazole, now used in the processes of diabetes and parasitic infections, are presented as antineoplastic effects in studies of various types of cancer. For metformin, it is possible that anticancer mechanisms of action, among others, may be made viable by LKB1 / AMPK / mTOR. Mebendazole prevents the polymerization of tubulins, inhibiting the growth and invasiveness of cancer cells. Thus, the present study has as a preventive effect metformin and mebendazole, known for their anti-neoplastic antibodies and low toxicity, in isolation and in combination with AGP01 (prescribed from neoplastic cells present in the patient with gastric ascites fluid of the intestinal type). This study is in vitro: MTT cytotoxicity, viability / apoptosis and necrosis assessment, cell cycle analysis and migration assay. One metfomine had 6.2mM IC50 and the 300mM IC50 mebendazole given alone, when combined with a new level of new IC50 values of 1.8mM and 88nM, respectively. The cell migration was inhibited for the metformin from the time of 12h and mebendazole from the time of 24h, a combination of the drugs showed no change in the time of inhibition, but increased the reliability of the test. Mebendazole and metformin induced cell death by apoptosis and prevented cell cycle progression, increasing the percentage of cells in the G1 / G0 phase and decreasing the percentage of cells in the S phase and G2 / M phase. These data confirm, at least in the antineoplastic effects of these drugs.Item Acesso aberto (Open Access) Papel do gene PIWIL1 como possível agente no processo de transição epitélio-mesenquimal no câncer gástrico(Universidade Federal do Pará, 2019) PAIVA, Juliana Albuquerque Pinto; KHAYAT, André Salim; http://lattes.cnpq.br/6305099258051586The PIWI-LIKE PROTEIN 1 (PIWIL1) gene has emerged as an attractive target for gastric cancer, as studies have shown that PIWIL1 protein is expressed at increased levels in cancer tissues, stem cells and germ cells, but it has been shown to be absent in normal somatic tissues. This means that it could be a potential target for therapy, since most non-cancer cells would not be affected by cytotoxic effects. Although relevant information on the possible role of PIWIL1 in the carcinogenesis of gastric cancer is provided by the current literature, the molecular mechanisms involved in this carcinogenic process remain unclear. Therefore, in order to investigate the molecular mechanisms by which PIWIL1 confers advantages to cancer cells, CRISPR/Cas9 technology was employed in order to perform the permanent knockout of PIWIL1 gene in the AGP01 gastric cancer cell line. After knockout, experiments were carried out to evaluate the effect of this molecular alteration on the migration and invasion capacity of the cell line, as well as on the expression of genes involved in these two cellular mechanisms. The results demonstrated that PIWIL1 gene knockout caused a significant decrease in the migration capacity of AGP01 after 24 hours, as well as a significant decrease in the cell invasion capacity. In addition, gene expression results revealed 26 genes (five overexpressed and 21 hypoexpressed - when comparing the cell lines before and after knockout) that encode proteins involved in invasion and migration cellular processes. According to the current literature, nine of these 26 genes (DOCK2, ZNF503, PDE4D, ABL1, ABL2, LPAR1, SMAD2, WASF3 and DACH1) are possibly related to the mechanisms used by PIWIL1 to promote carcinogenic effects related to migration and invasion, since their functions are consistent with the observed modification (being overexpressed or hypoexpressed after knockout). Taken together, these data reinforce the idea that PIWIL1 should play a crucial role in the gastric cancer signaling pathway, regulating several genes involved in the migration and invasion processes, so its use as a therapeutic target can generate promising results in the treatment of this type of cancer.